Cheng H W, Rafols J A, Goshgarian H G, Anavi Y, Tong J, McNeill T H
Division of Neurogerontology, Andrus Gerontology Center, University of Southern California, Los Angeles 90089-0191, USA.
Exp Neurol. 1997 Oct;147(2):287-98. doi: 10.1006/exnr.1997.6618.
Golgi-Cox method and morphometric analyses were used to study the plasticity of striatal medium spiny I neurons in 6-month-old C57BL/6N mice after unilateral or bilateral lesion of the cerebral cortex or combined lesions of the ipsilateral cerebral cortex and intralaminar thalamus. In adult mouse, unilateral lesions of the cerebral cortex did not result in a net gain or loss of linear dendritic length in a randomly selected population of striatal medium spiny I neurons. In addition, there was a well-defined time course of striatal spine loss and replacement occurring after a unilateral cortical lesion. By day 3 postlesion the average 20-microm dendritic segment had lost 30% of the unlesioned control spine value, reached its nadir, lost 45.5%, at 10 days postlesion, and recovered to 80% of unlesioned control levels by 20 days postlesion. The recovery of spines was blocked by a secondary lesion on the contralateral cortex but not on the ipsilateral intralaminar thalamus. These data suggest that striatal medium spiny I neurons of adult mice have a remarkable capacity for plasticity and reactive synaptogenesis following a decortication. The recovery of spine density is primarily induced by axonal sprouting of survival homologous afferent fibers from the contralateral cortex.
采用高尔基-考克斯法和形态计量学分析,研究6月龄C57BL/6N小鼠在单侧或双侧大脑皮质损伤或同侧大脑皮质与层内核丘脑联合损伤后纹状体中等棘状I型神经元的可塑性。在成年小鼠中,单侧大脑皮质损伤并未导致随机选择的纹状体中等棘状I型神经元群体的线性树突长度出现净增加或减少。此外,单侧皮质损伤后,纹状体棘突丢失和替换存在明确的时间进程。损伤后第3天,平均20微米的树突段失去了未损伤对照棘突值的30%,达到最低点,在损伤后10天失去45.5%,并在损伤后20天恢复到未损伤对照水平的80%。对侧皮质的二次损伤会阻止棘突的恢复,但同侧层内核丘脑的二次损伤则不会。这些数据表明,成年小鼠的纹状体中等棘状I型神经元在去皮质后具有显著的可塑性和反应性突触形成能力。棘突密度的恢复主要是由对侧皮质存活的同源传入纤维的轴突发芽诱导的。